Recent studies focusing on NFY activity and heat shock 70 kDa protein 1A (HSPA1A) expression in the brain of a Huntington's disease (HD) mouse model have shown that mutant Huntingtin (Htt) aggregates sequester NFYA and NFYC leading to the reduction of HSPA1A gene expression, indicating NFY components as modulators of the HD pathological process [14]. This evidence concerns the gene HTT and juvenile Huntington disease.